Our overall objective is to improve understanding of the cellular and molecular means by which pulmonary endothelial cells participate in determining the quality of systemic arterial blood. Within this broad scope, our special interests are in the means by which surface enzymes of pulmonary endothelial cells determine which polypeptide hormones and related substances gain access to arterial blood and which do not. In particular, we will examine for the cellular and subcellular dispositions of aminopeptidase M (N), aminopeptidase P and dipeptidyl aminopeptidase IV, all enzymes postulated to occur on the pulmonary vascular surface and all enzymes postulated to metabolize one or more of bradykinin, kallidin, substance P, enkephalins and higher homologs, and angiotensins I, II or III. As a new initiative, we propose to examine for participation of pulmonary endothelium in the entrapmen and disposal of sieved particulates. Special focus will be placed on the ability of endothelium to transform itself from an immunologically privileged, antithrombogenic tissue into a tissue that participates actively in thrombus formation and complement-linked reactions. What we seek are structure-function correlates of such transformations, especially as induced by phagocytosis and viral infection. By pursuing these specific aims, it should be possible further to elucidate the dynamic cell biology of pulmonary endothelium and to relate such knowledge to the overall performance of the lungs.